ArticlePLoS biology2019
Mediator MED23 regulates inflammatory responses and liver fibrosis.
Article in PLoS biology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 17 citations in OpenAlex.
- Unraveling the HGF/MET axis in Mallory-Denk body pathogenesis associated with liver fibrosis through single-cell transcriptomics.Signal transduction and targeted therapy · 2026Article
- Targeting MED23 inhibits hepatocellular carcinoma development by suppressing compensatory proliferation and facilitating ROS-mediated cell death.Cell death & disease · 2025Article
- The Mediator Complex: A Regulatory Hub for Transcriptional Activity of Nuclear Receptors.Cells · 2025Review
- A phosphorylation switch in the Mediator MED15 controls cellular senescence and cognitive decline.Cell discovery · 2025Article
- Mediator complex subunit MED23 dampens antiviral innate immunity by restricting RIG-I expression.PLoS biology · 2025Article
- Mediator MED23 controls oligodendrogenesis and myelination by modulating Sp1/P300-directed gene programs.Cell discovery · 2024Article
- Article
- Med23 deficiency reprograms the tumor microenvironment to promote lung tumorigenesis.British journal of cancer · 2024Article
- ADRB2 serves as a novel biomarker and attenuates alcoholic hepatitis via the SIRT1/PGC-1α/PPARα pathway: integration of WGCNA, machine learning and experimental validation.Frontiers in pharmacology · 2024Article
- Genetically Engineered Mice Unveil In Vivo Roles of the Mediator Complex.International journal of molecular sciences · 2023Review
- Mediator complex subunit 8 is a prognostic biomarker in hepatocellular carcinoma.American journal of translational research · 2022Article
- Mediator complex proximal Tail subunit MED30 is critical for Mediator core stability and cardiomyocyte transcriptional network.PLoS genetics · 2021Article
- EZH2-mediated inhibition of KLF14 expression promotes HSCs activation and liver fibrosis by downregulating PPARγ.Cell proliferation · 2021Article
- Effect of acupuncture combined with Shenqi Yigan Decoction on liver function and T cell subsets in patients with HBV-induced liver fibrosis.American journal of translational research · 2021Article
- Co-delivery of miR-29b and germacrone based on cyclic RGD-modified nanoparticles for liver fibrosis therapy.Journal of nanobiotechnology · 2020Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Liver fibrosis, often associated with cirrhosis and hepatocellular carcinomas, is characterized by hepatic damage, an inflammatory response, and hepatic stellate cell (HSC) activation, although the underlying mechanisms are largely unknown. Here, we show that the transcriptional Mediator complex subunit 23 (MED23) participates in the development of experimental liver fibrosis. Compared with their control littermates, mice with hepatic Med23 deletion exhibited aggravated carbon tetrachloride (CCl4)-induced liver fibrosis, with enhanced chemokine production and inflammatory infiltration as well as increased hepatocyte regeneration. Mechanistically, the orphan nuclear receptor RAR-related orphan receptor alpha (RORα) activates the expression of the liver fibrosis-related chemokines C-C motif chemokine ligand 5 (CCL5) and C-X-C motif chemokine ligand 10 (CXCL10), which is suppressed by the Mediator subunit MED23. We further found that the inhibition of Ccl5 and Cxcl10 expression by MED23 likely occurs because of G9a (also known as euchromatic histone-lysine N-methyltransferase 2 [EHMT2])-mediated H3K9 dimethylation of the target promoters. Collectively, these findings reveal hepatic MED23 as a key modulator of chemokine production and inflammatory responses and define the MED23-CCL5/CXCL10 axis as a potential target for clinical intervention in liver fibrosis.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.